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INTRODUCTION

Although it might appear deceptively simple, it is not always easy to sclerose a varicose vein. Even a small amount of damage will produce intravascular thrombus, but thrombosis alone usually does not obliterate the vessel. Intact endothelium contains tissue plasminogen activator that can dissolve thrombus. A thrombosed vessel with intact endothelium will simply recanalize.

Vascular fibrosis and obliteration only occur in response to irreversible endothelial cellular destruction. If an injected sclerosant is too weak, the vessel may initially close, but recanalization will occur and an incompetent pathway for reflux then persists. If the injected sclerosant is too strong, the varicose vessel endothelium is destroyed, but the sclerosant will also affect adjacent normal vessels causing damage there as well. The goal is to deliver a minimum volume and concentration of sclerosant that will cause irreversible damage to the endothelium of the abnormal vessel to be sclerosed, while leaving adjacent normal vessels unaffected.

No single sclerosing agent can provide perfect results in every clinical setting. There are not only significant differences between agents of different classes, but there are also important subtle differences between agents of the same class that at first glance seem very similar. There is also a great deal of individual variability in response to sclerosing solutions. The clinician must be prepared to work with a variety of agents to meet the needs of circumstance. The choice of which sclerosing agent to use is based on a good understanding of the mechanism of action of each sclerosing solution.

Virtually, any foreign substance can cause venous endothelial damage. Historical methods for producing venous endothelial trauma have included “a slender rod of iron” (reportedly used by Hippocrates himself), phenol, absolute alcohol, ferric chloride, anti-syphilitic mercurial drugs, and hundreds of other agents. These early sclerosing agents caused many deaths in addition to a high incidence of local tissue necrosis, pain, failed sclerosis, and allergic reactions.

An ideal sclerosing solution would have no systemic toxicity. It would produce local endothelial destruction extending all the way to the adventitia with a minimum of thrombus formation. Because all sclerosants eventually flow into the deep system, an ideal sclerosant would be rapidly inactivated by dilution. It would require a long period of contact to be effective, making it more effective in areas of stasis and safer in normal veins where there is a high flow. It would be nonallergenic. It would be strong enough to sclerose even the largest vessels, yet it would produce no local tissue injury if extravasated. It would not cause staining or scarring, nor telangiectatic matting. It would be perfectly soluble in normal saline. It would be painless upon injection, inexpensive, and approved by the US Food and Drug Administration (FDA).

The ideal sclerosant does not yet exist, but modern sclerosants can exhibit near-ideal behavior when used correctly. The degree of endothelial cell destruction can often be tempered by ...

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